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. Author manuscript; available in PMC: 2015 Jul 8.
Published in final edited form as: Annu Rev Neurosci. 2014 Jul 8;37:161–181. doi: 10.1146/annurev-neuro-071013-014111

Figure 4.

Figure 4

Proposed model of nonlinear neurovascular coupling incorporating fast and slow propagated vasodilation. Neuronal activity at the capillary level could either directly or indirectly cause an increase in endothelial intracellular calcium. An initial large-amplitude increase in endothelial calcium could initiate endothelial hyperpolarization, which would be rapidly propagated with minimal attenuation to drive relaxation of perivascular SMCs all the way up to the pial arteries (Wölfle et al. 2011). The same initial increase in endothelial calcium could also drive a slower propagating wave of increased calcium within the endothelium (Tallini et al. 2007), bringing NO and prostanoid-dependent vasodilation over a shorter distance. Combined, these two effects would generate spatiotemporal nonlinearities consistent with the properties of functional hyperemia. A lower threshold in endothelial calcium (Marrelli 2001) for slow propagation might explain continued parenchymal hyperemia, but only transient (initial) long-range dilation as shown in Figure 2.